title: Differences in characteristics of men with localised prostate cancer who demonstrate low, intermediate or high prostate-specific antigen velocity.
abstract: BACKGROUND
  Current diagnostic tools are inadequate for reliable prediction of prostate cancer (PCa) aggressiveness in patients with localised disease. This results in many patients being exposed to potentially unnecessary invasive treatment and its associated morbidities. In order to develop appropriate treatment strategies, it is essential to understand the differences between patients who will develop aggressive disease and those who will not.
  
  
  METHODS
  A longitudinal study was conducted in men with localised PCa on active surveillance for their disease in which 140 subjects were followed every 3 months for up to 5 years. Change in prostate-specific antigen (PSA) over time (PSA velocity) was used as a marker for PCa progression. Subjects were categorised as slow, intermediate and fast progressors based on tertiles of PSA velocity. Differences in baseline markers were investigated using logistic regressions. Two approaches were used, slow progressors were compared with fast progressors (model 1) and slow progressors were compared with combination of intermediate and fast progressors (model 2).
  
  
  RESULTS
  Aspirin was negatively associated with high PSA velocity in model 1 (odds ratio (95% confidence interval): 0.24 (0.06, 0.94), P-value = 0.04) and model 2 (odds ratio = 0.22 (0.08, 0.59), P-value = 0.003), whereas smoking was positively associated with high PSA velocity in model 1 (1.03 (0.92, 1.13), P-value = 0.01).
  
  
  CONCLUSIONS
  These findings highlight the role of aspirin and smoking in PCa progression. They have potential towards risk stratification as well as PCa prevention and hence need to be investigated further.
authors.affiliation: Arizona Cancer, Tucson, Arizona, USA. algotar@email.arizona.edu
authors.forename: A M
authors.initials: AM
authors.lastname: Algotar
authors.forename: P A
authors.initials: PA
authors.lastname: Thompson
authors.forename: J
authors.initials: J
authors.lastname: Ranger-Moore
authors.forename: M S
authors.initials: MS
authors.lastname: Stratton
authors.forename: C H
authors.initials: CH
authors.lastname: Hsu
authors.forename: F R
authors.initials: FR
authors.lastname: Ahmann
authors.forename: R B
authors.initials: RB
authors.lastname: Nagle
authors.forename: S P
authors.initials: SP
authors.lastname: Stratton
mesh_terms: D000328:Adult; D000368:Aged; D001241:Aspirin / Q000009:adverse effects*; D014408:Biomarkers, Tumor / Q000097:blood*; D018450:Disease Progression; D005500:Follow-Up Studies; D006801:Humans; D007610:Kallikreins / Q000097:blood*; D008137:Longitudinal Studies; D008297:Male; D008875:Middle Aged; D017430:Prostate-Specific Antigen / Q000097:blood*; D011471:Prostatic Neoplasms / Q000175:diagnosis* / Q000453:epidemiology; D012307:Risk Factors; D012907:Smoking / Q000009:adverse effects*
chemical_list: D014408:Biomarkers, Tumor; C549870:KLK3 protein, human; D007610:Kallikreins; D017430:Prostate-Specific Antigen; D001241:Aspirin